Transcriptomics

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Adaptaquin is an inhibitor of oxygen-sensing prolyl-hydroxylase domain enzymes that abrogates ATF4-dependent death and improves outcomes from brain hemorrhage


ABSTRACT: Disability or death secondary to intracerebral hemorrhage (ICH) is attributed to blood lysis, liberation of iron and generation of oxidative stress. Iron chelators bind free iron and prevent neuronal death induced by oxidative stress and disability due to ICH, but the mechanisms remain unclear. Here we show that the hypoxia-inducible factor prolylhydroxylase (HIF PHD) family of iron-dependent oxygen sensors is an effector of iron chelation in abrogating ICH-induced death. Molecular reduction of the three HIF PHD isoforms in mouse striatum improves functional recovery following ICH. A low molecular weight, hydroxyquinoline inhibitor of the HIF PHDs, which we call adaptaquin, reduces neuronal death and behavioral deficits following ICH in distinct rodent models. Unexpectedly, adaptaquin protects from oxidative death by suppressing ATF4- dependent prodeath gene expression rather than by activating a HIF-dependent prosurvival pathway.

ORGANISM(S): Mus musculus

PROVIDER: GSE75048 | GEO | 2016/03/01

SECONDARY ACCESSION(S): PRJNA302291

REPOSITORIES: GEO

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